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Semiology > Finals > Flashcards

Finals Flashcards

1
Q

Fever (Pyrexia) characteristics

A
  • equal or above 37.3°C in morning, equal or above 37.8°C in evening
  • common
  • may mask malignant or non- malignant haematology disorder
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2
Q

Pathophysiology of fever

A
  • febrile response to endogenous pyrogens (cytokines) in response to exogenous pyrogens (micro- organisms or toxins)
  • endogenous pyrogens act on thermo sensitive neurons in hypothalamus, upgrade set point via prostaglandins
  • body reacts with heat production
  • chemotaxis of neutrophils, adhesion and diapedesis of vessel endothelium, proliferation t-lymphocytes, release cytokines, histamine, leukotrienes, prostaglandins, tissue necrosis (eventually)
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3
Q

Pel- Ebstein Fever

A
  • condition in Hodgkin’s lymphoma
  • fever that cyclically decrease and increase over average of 1-2 weeks
  • B symptoms
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4
Q

What is a major cause of pyrexia?

A

• infectious diseases in immunosuppressed haematology patients

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5
Q

What do immunosuppressed haematologic patients with pyrexia need for immediate treatment?

A

empiric broad spectrum antibiotics

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6
Q

Where do Infectious diseases commonly occur?

A
  • Neutropenic patients
  • Lymphoma- Mutliple Myeloma

• non- malignant haematology disorders (thalassemia- sickle cell disease)

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7
Q

What is impaired in infectious diseases in immunosuppresed haematologic patients

A
  • cellular response (decreases granulocytes)

* immune response (decreased immunoglobulin levels)

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8
Q

What does Chemotherapy/Radiotherapy do to normal tissue

A

• destruction of normal mucosal tissue in gastro- intestinal, sinuses and urinary tract systems

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9
Q

What are drugs that lead to immunosuppresion

A
  • corticosteroids
  • Fludarabine (CLL treatment)
  • Idarubicine- cytarabine ( AML treatment)
  • high dose methotrexate (Lymphoma treatment)
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10
Q

if AFP increased, what could be suspected?

A

cancer in liver

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11
Q

what is AFP?

A
  • α fetoprotein
  • protein made in liver of developing baby
  • used to detect birth defects and genetic disorders (down syndrome, neural tube defects)
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12
Q

Portal hypertension

A

• increase in blood pressure around liver
→ portal venous system
→ veins from stomach, intestine, spleen, pancreas merge into portal vein → then branch into liver

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13
Q

What Hepatic Vein Pressure Gradient indicates Portal Hypertension?

A

if more than 5mm Hg

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14
Q

How is the Wedge HVP, Free HVP and HVPG in Posthepatic portal hypertension?

A

WHVP increased
FHVP increased
HVPG normal

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15
Q

What is HVPG?

A
  • Hepatic Vein Pressure Gradient

* difference between wedged and free hepatic venous pressures

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16
Q

What are esophageal varices??

A
  • extremely dilated sub mucosal veins in lower third of esophagus
  • consequence of portal hypertension due to cirrhosis
  • can lead to severe bleeding in affected patients
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17
Q

What are causes of portal hypertension?

A
  • ↑atrial pressure (constrictive pericarditis)
  • IVC → webs, tumor onvasion, thrombosis
  • Hepatic veins → large due to thrombosis, web, tumor invasion
  • portal veim & splenic vein thrombosis or invasion, comrpession by tumor
  • incr blood flow → splenomegaly, idiopathic, arteriovenous fistula
  • Post-sinusoidal, sinusoidal, pre sinusoidal
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18
Q

Posthepatic diseases

A
  • Budd-Chiari syndrome
  • Constrictive pericarditis
  • inferior vena cava obstruction
  • right sided heart failure
  • severe tricuspid regurgitation
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19
Q

Intrahepatic diseases

A 
• presinusoidal
→ idiopathic portal hypertension
→ Primary biliary cholangitis
→ sarcoidosis
→ Schistosomiasis
• sinusoidal
→ alcoholic cirrhosis
→ alcoholic hepatitis
→ cryptogenic cirrhosis
→ postnecrotic cirrhosis
• Postsinusoidal
→ sinusoidal obstruction syndrome
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20
Q

Prehepatic

A

• portal vein or splenic vein thrombosis

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21
Q

Cirrhosis?

A
  • diffuse process with fibrosis, nodule formation replacing normal hepatic parenchyma
  • end result of fibrogenesis → occurs with chronic liver injury
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22
Q

Etiology cirrhosis

A
  • US → alcohol, hepatitis C
  • 27.000 death / year
  • reduced life expectancy
  • obesity, drugs, age, male, chronic HBV / HCV, iron (hemachromatosis), α-1-antitrypsin, metabolic syndrome, drugs
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23
Q

Causes of Clubbing

A

• thoracic and non thoracic
• thoracic: bronchitis, empyema, lung abscess, cystic fibrosis, lung Ca, Esophageal Ca, mesothelioma, Bac. Endocarditis
→ interstitial lung disease: asbestosis, fibrosis alveolitis
→ vascular causes: AV malformation, cyanotic heart disease

• non thoracic: hepatic cirrhosis, ulcerative colitis, crohn’s disease

24
Q

What are complications of cirrhosis?

A
  • ascites
  • spontaneous bacterial peritonitis
  • hepatorenal syndrome
  • variceal hemorrhage
  • hepatic encephalopathy
  • hepatocellular carcinoma
25
Q

Ascites?

A
  • accumulation of fluid within peritoneal cavity
  • common
  • 2 yr survival of patients with ascites approx 50 percent
  • Grade I: mild, detectable
  • Grade II: moderate, symmetrical distention
  • Grade III: large gross ascites with marked abdominal distension
26
Q

Puddle Sign

A

• prone 3-5 min, then rises to all fours
• stethoscope on area of abdomen
• flicking finger over localized flank area
→ move stethoscope to opposite flank
→ sudden increase in intensity is positive sign

27
Q

Stages of ascites

A
  • No ascites
  • uncomplicated ascites
  • ascites and hyponatraemia
  • refractory ascites
  • hepatorenal syndrome
28
Q

Spontaneous bacterial peritonitis (SBP)

A

most common bacterial infection on hospitalized cirrhotic patients

29
Q

Unconjugated Hyperbilirubinemia Causes

A
  • ↑bilirubin production (prehepatic → hemolysis, ineffective erythropoiesis, blood transfusion, resoprtion of hematomas)
  • ↓ hepatocellular uptake of unconjugated bilirubin (drugs → rifampin, cyclosporine A)
  • ↓ bilirubin conjugation (autosomal inherited disorders)
30
Q

How does the bilirubin transport by hepatocyte occur?

A

??

31
Q

What is Chlestasis

A
  • stagnation, or marked reduction in bile secretion and flow
  • can be due to functional impairment of hepatocytes in secretion of bile and/ or due to obstruction at any level of excretory pathway of bile
  • from level of hepatic parenchymal cells at basolateral membrane of hepatocyte to ampulla of vater in duodenum
  • marke bile acidemia, normal to slightly elevated bilirubin
32
Q

name the two type of gallstones and describe them

A

• cholesterone stone
→ more than 80%
→ cholesterol monohydrate crystals
→ obese, women, race, estrogen, age

• pigment stones
→ 20%
→ black pigment stone ( calcium bilirubinate polymer, formed in gallbladder, chronic hemolysis (sickle cell anemia), crohn’s disease (ileal resection)
→ brown pigment stone ( cholesterol/fatty soap/ calcium bilirubinate, bile duct, chronic biliary tract infection, bacterial β-glucoronidase deconjugates bilirubin, biliary stasis)

33
Q

What is biliary colic?

A
  • symptoms of gallbladder stones
  • episodic attacks of severe pain in RUQ or epigastrium for at least 15-30min, radiating to right back or shoulder
  • pos reaction to analgesics

→ NSAISs, spasmolytics and opioids

34
Q

Cholecystitis

A

• inflammation of gallbladder

35
Q

what are signs and symptoms of chelcystitis

A
  • severe pain in RUQ or center abdomen
  • pain that spreads to right shoulder or back
  • tenderness over abdomen when touched
  • nausea
  • vomiting
  • fever
  • often after meal, esp. large and fatty
36
Q

Cholangitis

A
  • inflammation of bile duct system

* inflammation and fibrosis pf hepatobiliary system characterized by eventual narrowing and obstruction of bile ducts

37
Q

Into what categories is cholangitis divided into

A
  • primary sclerosing cholangitis
  • secondary cholangitis
  • immune cholangitis
38
Q

What sign and symptom has a high specificity for presence of acute cholangitis

A

Charcot’s triad
→ jaundice
→ fever with or without rigors
• RUQ abd pain

39
Q

What is included in the Reynolds pentad

A

• charcot’s triad, confusion, shock

40
Q

With what value of HVPG do varices develop?

A

> 10mmHg

41
Q

With what value of HVPG does one have a high risk of variceal bleeding?

A

> 12mmHg

42
Q

With what value of HVPG does one have a high risk of death

A

> 16mmHg

43
Q

With what value of HVPG does one have a high risk of treatment failure and rebleeding?

A

> 20mmHg

44
Q

With what value of HVPG does one have a 3% increase of death for the following 19month?

A

1mmHg

45
Q

What portal circulation is located in the retroperitoneum?

A

mesenteric veins

46
Q

What portal circulation is located in the umbilical (caput medusa)

A

• left portal via recannulated umbilical vein

47
Q

What portal circulation is located in the rectum?

A

• superior hemorrhoidal veins

48
Q

What portal circulation is located in the gastroesophageal junction?

A

• short gastric and left gastric (coronary) veins

49
Q

What does alcohol lead to in male patients?

A
  • in Testes: inhibition retinol to retinal, inhibition testosterone synthesis, down regulation LH and GABA receptors
  • Periphery: increased hepatic conversion to active estrogen forms, relative incr
50
Q

what is Sialadenosis?

A
  • uncommon benign non inflam and non neoplastic enlargement of salivary gland, usually parotid
  • associated with diabetes mellitus, malnutrition, liver cirrhosis due chronic alcoholism, hyperlipidemia, acromegaly
51
Q

Hepatic Encephalopathy

A

decline in brain function as result to severe liver disease, liver can’t remove toxins from blood toxin build up

52
Q

Pathophysiology of Hepatic Encephalopathy

A 
• Cerebral vasomotor dysfunction
• oedema sec to ammonia toxicity
• Inflam due to SIRS
• Putative benzodiazepine- like molecules
• Ammonia thought to be main factor
→ Ammonia converted to glutamine by liver, because ammonia clearance impaired
→ astrocyte swelling (↑Glu and Gln)
→ astrocyte dysfunction
→ neuronal dysfunction (↑GABA)
→ hepatic encephalopathy
53
Q

Stages of Hepatic Encephalopathy West Haven Scale:

A

0 Asterixis absent
I asterixis can be detected, lack awareness, hypersomnia
II obvious asterixis
III asterixis generally absent, bizarre behaviour, gross disorientation, stupor
IV coma

54
Q

What is feta hepaticus?

A
  • sour, musty, feculent smell of breath
  • presence of mercaptans (byproduct methionine metabolism)
  • liver trouble filtering toxins
55
Q

What is the role of the liver?

A
  • release of HDLP, VLDLP, Phospholipids, blood glucose, urea, uric acid, amino acids, coenzymes(: NAD, NADP, FMN, FDP, HS CoA, PALP), Bile, cholesterol, bile acids, bilirubin, blood plasma proteins
  • takin in of lactate, monosaccharides, AA, Lipids, Fatty acids, HDLP, Bilirubin,…
56
Q

Celiac disease

A

• gluten sensitive enteropathy or celiac sprue

Semiology (2 decks)

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